Key points are not available for this paper at this time.
BACKGROUND: Compensatory enlargement (CE) of atherosclerotic human arteries has been reported; however, the pattern of arterial remodeling in response to plaque formation is not unique. HYPOTHESIS: The study was undertaken to determine the extent of coronary artery compensatory enlargement at stenotic lesions and to correlate the arterial compensatory enlargement with risk factors. METHODS: We studied 62 patients with stable angina and de novo single-vessel disease using intravascular ultrasound and obtained good images in 42 patients (68%). The vessel cross-sectional area (VA), lumen cross-sectional area (LA), and plaque cross-sectional area (PA) were measured at the lesion site and at proximal and distal reference sites. Positive CE was defined as increase in VA of lesion site > 10% compared with that of proximal reference site (CE group, n = 15); shrinkage was defined as reduction in VA of lesion site > 10% compared with that of proximal reference site (S group, n = 14); inadequate CE was defined as intermediate between CE and S (IE group, n = 13). All subjects had coronary risk factors measured before this study. RESULTS: There was no difference in VA, LA, or PA among the three groups at the proximal and distal reference sites, nor in LA at the lesion site; however, VA and PA were significantly smaller in the S group than in the other groups (p < 0.01). Of coronary risk factors, increased systolic blood pressure (SBP), increased diastolic blood pressure (DBP), and decreased high-density lipoprotein cholesterol (HDL-c) levels had the strongest association with shrinkage (p < 0.05). CONCLUSION: Hypertension and decreased HDL level may contribute to the shrinkage response in middle-aged patients with stable angina.
Isoda et al. (Fri,) studied this question.